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Nutrition Research Newsletter, Oct, 2000
Obesity has been associated with low serum levels of 25-hydroxyvitamin D, which is related to increased plasma concentrations of immunoreactive parathyroid hormone (PTH). Several assumptions have been made regarding the increased risk of vitamin D deficiency in obesity. Obese individuals may avoid exposure to sunlight, which is essential for the cutaneous synthesis of vitamin [D.sub.3]. It has also been suggested that the metabolic clearance of vitamin D may increase in obesity, possibly with enhanced uptake of adipose tissue.
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To determine why obese individuals are prone to vitamin D deficiency, researchers from Boston University's School of Medicine conducted a series of studies to determine their capability to handle vitamin D originating from either the oral route or from the skin. The study also tested the effect obesity has on the intestinal absorption of vitamin [D.sub.2] (ergocalciferol).
Thirteen healthy subjects of normal body weight (BMI [is greater than or equal to]25) and 13 healthy obese subjects (BMI [is greater than] 30) were included in this study. The study was performed during the winter so that subjects refrained from sunlight exposure. The study of cutaneous vitamin [D.sub.3] synthesis (cholecalciferol) in response to UV-B irradiation was performed by submitting the subjects to whole-body irradiation in a phototherapy unit that emits wavelengths of 260-330 nm. To study the response to an oral challenge with vitamin [D.sub.2], the subjects ingested 50,000 IU of ergocalciferol one month after the previous study.
Obese subjects had significantly lower basal 25-hydroxyvitamin D concentrations and higher PTH levels than did the control group. After the whole-body irradiation, the increase in vitamin [D.sub.3] levels was 57% lower in obese subjects. The content of the vitamin [D.sub.3] precursor, 7-dehydrocholesterol, in the skin of obese and non-obese subjects did not differ significantly between groups nor did its conversion to previtamin D3 after irradiation. After the oral dose of vitamin [D.sub.2], BMI was found to be inversely correlated with serum vitamin [D.sub.2] levels. However, peak blood concentrations of vitamin [D.sub.2] were not significantly different between the two groups.
Because humans obtain most of their vitamin D requirement from exposure to sunlight, the >50% decreased bioavailability of cutaneously synthesized vitamin D in the obese subjects could explain the increased vitamin [D.sub.3] deficiency in obese subjects. The orally supplied vitamin [D.sub.2] was more bioavailable, probably because after absorption, it is also sequestered in the large pool of body fat. Oral vitamin D should be able to correct the vitamin D deficiency associated with obesity, but larger doses than usual may be necessary.
Jacobo Wortsman, Lois Y. Matsuoka, Tai C. Chen, et al., Decreased Bioavailabiliy of Vitamin D in Obesity, Am J Clin Nutr 72:690-693 (September 2000) [Correspondence: M. F. Holick, Boston University School of Medicine, 715 Albany St., M1013, Boston, MA 02118. E-mail: mfholick@bu.edu.]
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